The present invention refers to compositions based on amino acids, in particular for oral or parenteral use, suitable for the treatment of the heart insufficiency. National statistics indicate that, in the USA, chronic heart failure (CHF) incidence and prevalence have increased over the last twenty years, despite the increased resources devoted to its prevention (Sytkowski P. A. et al.; New England Journal of Medicine, 1990; 322: 1635-1641), and the significant progresses in availability of treatment of this particular disease (Pitt B. et al.; New England Journal of Medicine, 1999; 341: 709-717).
Chronic heart failure is no longer strictly deemed as the consequence of hypertension or valvular heart disease, but rather of coronary heart disease, and therefore of arteriosclerosis (Gheorghiade M. and Bonow R. O.; Circulation, 1998; 97: 282-289).
In all the patients suffering this disease, intolerance to physical exercise is one of the major clinical feature, which is consistent with the proceeding of the same pathology; in addition, a noticeable skeletal muscle atrophy, often in the absence of signs of severe malnutrition, is a quite constant accompanying feature of chronic heart failure of any grade (Mancini D. M. et al.; Circulation, 1992, 85: 1364-1373).
Mechanisms of muscle wasting have been recently reviewed in literature (Mitch W. E. and Goldberg A. L.; New England Journal of Medicine, 1996; 355: 1897-1905.
It has not yet been clarified whether metabolic abnormalities observed during local physical exercise are functionally associated with alterations detected in the systemic exercise (Okita K. et al.; Circulation, 1998; 98: 1886-1891), although a recent study concluded that, most probably, intrinsic differences in skeletal muscle metabolism, rather than vasodilatory dynamics, must be taken into account for explaining the increased metabolic responses of glycolitic type in moderate physical strain of CHF patients.
On the contrary, in strenuously exercising skeletal muscles, the enhanced vasoconstriction following inability to increase the vascular conductance, is the main reason of exertional fatigue, despite normal pressor response (Shoemaker J. K.; Circulation, 1999; 99: 3002-3008).
There is no therapeutic approach based on the clinical evidences described above.
Till now, in fact, the only therapeutic intervention that has proved unequivocally to be beneficial in improving symptoms and prolonging life in patients with chronic heart failure was is that one with ACE inhibitors (Bart B. A. et al.; Journal of the American College of Cardiology, 1997; 30: 1002-1008, e Gheorghiade M. and Bonow R. O.; Circulation, 1998; 97: 282-289), further improved by the more extensive beta receptor blockade given by spironolactones, as recently published (Pitt B. et al.; New England Journal of Medicine, 1999; 341: 709-717). Both drugs are mainly anti-hypertensive agents.